A new study recently published in the journal Respirology reviewed the growing evidence of a link between cigarette smoking and the development of interstitial lung diseases (ILD) including idiopathic pulmonary fibrosis (IPF). The study is entitled “Smoking-related idiopathic interstitial pneumonia: A review” and was developed by researchers at the University Hospital of Heraklion in Greece and San Giuseppe Hospital-Multimedica in Italy.
ILD comprises a group of diseases that cause progressive scarring of lung tissue, compromising respiratory function and blood oxygenation. During the last decade, cigarette smoking has been associated with the development of diffuse interstitial lung diseases, including IPF, a progressive fatal lung disease of unknown origin in which the alveoli and the lung tissue are damaged, becoming thick and scarred (fibrosis), leading to severe breathing difficulties and compromising oxygen transfer between the lungs and the bloodstream. IPF is characterized by a shortness of breath that gradually worsens, with respiratory failure being the main cause of death. There is no cure for IPF and it is estimated that almost 130,000 individuals in the United States and 5 million worldwide suffer from the disease. IPF has a poor prognosis and around two-thirds of patients die within five years after being diagnosed.
In the study, researchers conducted a review focused on smoking-related lung damage, either inflammatory or fibrotic, and the clinical aspects of the associated disorders.
According to the authors, cigarette smoking leads to an exaggerated accumulation of inflammatory cells in the small airways and interstitium (the tissue and space surrounding the air sacs of the lungs). Smoking also triggers the production of transforming growth factor (TGF)-beta 1, a molecule that plays a central role in the development of lung fibrosis.
Smoking has been linked to telomere shortening. Telomeres are the caps at the end of each DNA strand in chromosomes, which protect the edge of the chromosomes from degradation and from fusion with other chromosomes. Short telomeres have been reported to be a risk factor for IPF development being associated with disease progression and an inability of the lung epithelium to regenerate. Smoking has also been associated with a dysregulation of autophagy (“self-eating”), a system in which cellular waste (harmful or dysfunctional cellular components but also pathogens) is specifically identified and eliminated. Autophagy has been reported to be decreased in lungs of IPF patients, which may lead to an increased accumulation of harmful particles and bacteria.
The research team concluded that cigarette smoking is involved in the development of ILD including IPF, although the exact mechanisms are still not clear. The team suggests that smoking cessation and prevention are crucial to improving IPF patients’ quality of life.